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hand and foot fracture and managementTRANSCRIPT
Fractures
Definitions
Dislocation = total loss of congruity between articular surfaces
Subluxation = partial loss of congruity between articular surfaces
Fracture = a break in continuity of a bone
Fracture healing
Fractures heal by restoration of bone continuity
Rate of healing varies with age and is quicker in children
Cancellous bone heals more quickly than cortical bone
Some movement at fractures site is required for healing to occur
Also requires an uninterrupted blood supply
Bone healing can arbitrarily be divided in to five stages
Stage one
Haematoma formation
Bone ends bleed
Periosteum is stripped for variable length
Surrounding soft tissues may be damaged
Stage two
Acute inflammation
Cell division begins within 8 hours
Cell proliferation seen within periosteum
Stage three
Callus formation
Dead bone is resorbed
Immature woven bone is laid down
Stage four
Woven bone is replaced by lamellar bone
Fracture becomes united
Stage five
Phase of remodelling
Medullary cavity is restored
Bone returns to normal shape
Principles of fracture management
Some general principles need to be applied to fracture management
Need to consider
o Reduction of the fracture
o Immobilisation of the fracture
o Rehabilitation
Need for reduction varies from fracture to fracture
Usually need to correct rotational or valgus or varus deformity
Intra-articular fractures need anatomical reduction
Reduction can be performed as either an open or closed procedure
Immobilisation is required until fracture union
Can be performed by external or internal methods
External methods include
o Plaster casts
o Traction
o External fixation
Internal methods include
o Plates
o Intramedullary nails
o K-wires
Indications for internal fixation
Intra-articular fractures - to stabilise anatomical reduction
Repair of blood vessels and nerves - to protect vascular and nerve repair
Multiple injuries
Elderly patients - to allow early mobilisation
Long bone fractures - tibia, femur and humerus
Failure of conservative management
Pathological fractures
Fractures that require open reduction
Unstable fractures
Complications of internal fixation
Infection
Non-union
Implant failure
Refracture
Indications for external fixation
Acute trauma - open and unstable fractures
Non union of fractures
Arthrodesis
Correction of joint contracture
Filling of segmental limb defects - trauma, tumour and osteomyelitis
Limb lengthening
Complications of external fixation
Overdistraction
Pin-tract infection
Complications of fractures
Early
o Infection
o Muscle and tendon injuries
o Nerve injuries
o Vascular injuries
o Visceral injuries
Late
o Delayed union
o Non-union
o Malunion
o Avascular necrosis
o Myositis ossificans
o Volkmann's contracture
o Stiffness and instability
o Algodystrophy
o Reflex sympathetic dystrophy
Compound fractures
All open fractures must be assumed to be contaminated
Object of treatment is to prevent them becoming infected
First aid treatment is the same as for a closed fracture
Peripheral neurovascular status should be assessed
In addition the wound should be covered with a sterile dressing
Wound should be photographed so that repeated uncovering is avoided repeated exposure
Antibiotic prophylaxis should be given
Tetanus immunisation status should be evaluated
Picture provided by Matteo Bianchi, Trauma Centre San Paolo, Milan, Italy
Management
Open fractures require early operation
Ideally this should be performed within 6 hours of injury
Aims of surgery are to:
o Clean the wound
o Remove devitalised tissue
o Stabilise the fracture
Small clean wounds can be sutures
Large dirty wounds should be debrided and left open
Debrided wounds can be closed by delayed primary suture ar 5 days
Pathological fractures
Generalised bone disease
o Osteoporosis
o Metabolic bone disease - osteomalacia, hyperparathyroidism
o Paget's disease
o Myelomatosis
Localised benign bone disorder
o Chronic infection
o Solitary bone cyst
o Fibrous cortical defect
o Chondroma
Primary malignant bone tumours
o Osteosarcoma
o Chondrosarcoma
o Ewing's tumour
Bibliography
Forward D, Morgan C G. Diagnosis and immediate care of open fractures. Hosp Med 2002; 63:
298-299.
Delayed and non-union
Union and consolidation
Fracture repair is a continuous process
The stages into which it is divided is an arbitrary process
Union should be regarded as incomplete repair
Present when an ensheathing callus is formed
Fracture site is still tender
Minimal movement at the fracture site is present
Consolidation should be regarded as complete repair
Radiologically fracture line is obliterated
Fracture site is non-tender
No movement is possible at the fracture site
Time to union and consolidation depends on many factors including
o Age
o Fracture type
o Blood supply
Fractures heal quicker in children
Upper limb fractures heal quicker than lower limb
Spiral fractures heal quicker than transverse fractures
Delayed union
Delayed union is the prolongation of time to fracture union
No definite timetable to define delayed union exists
Delayed union is due to
o Inadequate blood supply
o Infection
o Incorrect splintage
o Intact fellow bone
Clinical features
Fracture site remains tender
Bone may still move when stressed
On x-ray the fracture remains visible
May be little callus formation or periosteal reaction
Management
Usually continue previous treatment of fracture
May need to replace cast or reduce traction
Functional bracing promotes bone union
For tibial fracture may need to excise portion of fibula
It union is delayed more than 6 months may need to consider
o Internal fixation
o Bone grafting
Non-union
Non-union has many causes including:
o Bone or soft tissue loss
o Soft tissue interposition
o Poor blood supply
o Infection
o Pathological fracture
o Poor splintage or fixation
o Fracture distraction
Clinical features
Movement remains present at the fracture site
Movement is often relatively painless
Radiologically the fracture is still visible
Bone ends on either side of the fracture are sclerosed
Non-union can be either hypertrophic or atrophic
Management
Non-union is occasionally symptomless
Asymptomatic non-union may not require active treatment except splintage
For hypertrophic non-union internal or external fixation may lead to union
For atrophic non-union bone grafting is often required
Myositis ossificans
Due to heterotopic ossification with an muscle
Elbow is the commonest joint involved
Seen following dislocation or muscle rupture
Also occurs without injury in unconscious or paraplegic patients
Pain is an early symptom
Stiffness and reduced range of movement are late features
In the late stage of the process a bony lump is often palpable
Early x-ray shows fluffy calcification
Late x-ray shows none formation
Management
Rest joint in position of function
Once pain settles begin mobilisation
After several months consider excision of bony mass
Avascular necrosis
Certain bony regions are prone to bone ischaemia and necrosis
These areas include
o Head of femur
o Proximal scaphoid
o Body of the talus
Interruption of blood supply by a fracture results in avascular necrosis
Pain due to fracture non-union is the main symptom
X-ray shows increase in bone density
Management
Surgical intervention required if there is a reduction in function
May require arthrodesis or arthroplasty
Bone grafting
Loss of bone can occur in several situations including
o Trauma
o Tumours
o Man-made prostheses
Bone grafts can be used to fill the defect
Classification of bone grafts
Autograft = bone from the same individual
Allograft = bone from another individual of the same species
Xenograft = bone from another species
Autografts
Autogenous bone is the best graft material
May only be available in a limited amount
Also not suitable for significant load bearing
Cancellous bone can be used to fill cavity defects
Cortical bone can be used to provide structural support
Forms scaffold into which osteoblasts and osteoclasts can grow
Osteoblast differentiation leads graft resorption
Stimulates local bone growth by the process of osteoinduction
Remodelling occurs as load is applied to the graft
Harvesting of bone grafts
Bone can be harvested from the following sites
o Iliac crest
o Proximal tibia
o Distal radius
Iliac crest is the most common but its use is associated with significant morbidity
Cortico-cancellous grafts are harvested as strips
Cancellous bone can be taken from the inner or outer table
Vascularised grafts
Segments of bone can be transplanted as free vascularised grafts
Local rotational bone grafts may also be used
Blood supply to the graft is maintained
Technically difficult to perform
Results are unpredictable
Allografts
Allograft bone is more plentiful
Can be harvested from living donors or cadavers
Donor site morbidity is eliminated
Cadaveric bone and femoral heads are stored in tissue banks
Bone is frozen at -20 to -86 degrees
Freeze drying and storage at room temperature is occasionally used
Used in reconstruction after:
o Tumour resection
o Revision hip surgery
Infection is the major concern with the used of allografts
Bacterial contamination may occur, especially with cadaveric grafts
Can be eliminated with irradiation of the graft
Viral contamination with hepatitis of HIV is a concern
Bone should be kept in quarantine and living donors tested 90 days post surgery
Allograft bone is available as:
o Morsellised bone for impaction grafting
o Strut grafts to cover cortical bone
o Massive allografts to replace significant proportions of native bone
Bone substitutes
Interest exists in artificial bone substitutes
Would eliminate supply and infection problems associated with auto and allografts
Possible bone substitutes include:
o Calcium triphosphate
o Hydroxyapatite
o Calcium carbonate
o Glass-based cements
Most bone substitutes are brittle
Unable to withstand significant load bearing
Common and eponymous fractures
Management of common fractures
Clavicle
o Rest in sling or collar and cuff for two weeks
o Active shoulder movement started after first week
Femur - trochanteric region
o Fixation with dynamic hip screw
o Early postoperative mobilisation is important
Femur - shaft
o Operative reduction usually required
o Internal fixation achieved with intramedullary nail
Fibula - shaft
o Protect limb in below knee walking cast for 3 weeks
Humerus - neck
o In elderly disregard fracture and concentrate on shoulder movement
o If fracture impacted begin mobilisation early
Humerus - supracondylar region
o Reduce by manipulation under anaesthesia
o Place in full length cast with elbow at 90 degrees
o Observe carefully distal circulation
Olecranon
o Undisplaced fractures need immobilisation in right angled arm plaster
o Displaced and comminuted fractures require internal fixation
o Internal fixation can be achieved with tension band wires
Patella
o Undisplaced fractures should be protected in full leg cast for 3 weeks
o Displaced fractures require internal fixation with screw or tension band wire
o Comminuted fractures may require patellectomy
Phalanges
o Undisplaced fractures should be strapped for 2-3 weeks
o Displaced fractures may require manipulation and external fixation
Radius - head
o If minimal displacement place in collar and cuff for 3 weeks
o If severely comminuted excise radial head
Scaphoid
o Immobilise in Scaphoid cast until fracture united
o If delayed union consider fixation with Herbert screw
Tibia - shaft
o Undisplaced fracture require immobilisation in full leg cast
o Displaced fractures may require internal fixation with intramedullary nail
Eponymous fractures
Bennett's fracture
o Intra-articular fracture of the base of the first metacarpal
o Usually requires open reduction and internal screw fixation
Colle's fractures
o Fracture of the distal radius with dorsal and radial angulation and backward
displacement
o Closed reduction should be followed by immobilisation in forearm cast for 6 weeks
o Position should be checked by radiography one week after injury
Galeazzi fracture
o Fracture of the radial shaft with dislocation of the inferior radio-ulnar joint
o Usually requires internal fixation of the radius
Monteggia fracture
o Fracture of the proximal ulna with anterior dislocation of the radial head
o Usually requires internal fixation of the ulna
o Radial head should be reduced or excised
Pott's fracture
o A general term applied to ankle fracture's
Smith's fracture
o Fracture of the distal radius with anterior displacement of the distal fragment
o Closed reduction may be successful
o If fails requires open reduction and fixation with a buttress plate
Bibliography
Krasin E, Goldwirth M, Gold A, Goodwin D R. Review of the current methods in
the diagnosis and treatment of scaphoid fractures. Postgrad Med J 2001; 77: 235-
237.
Hip fractures
Refers to fractures of the proximal femur
60,000 hip fractures occur per year in the United Kingdom
Mean age of patient is 80 years
Incidence increases exponentially above the age of 65 years
Main risk factors are female sex and osteoporosis
Clinical features
Usually occurs following a fall
Patient usually has other significant co-morbidity
Main symptom is hip pain and inability to weight bear
The leg is shortened and externally rotated
Diagnosis confirmed by AP and lateral x-ray
Impacted undisplaced fractures may present diagnostic difficulty
Garden classification
Stage 1 - incomplete or impacted fracture
Stage 2 - complete fracture with no displacement
Stage 3 - complete fracture with partial displacement
Stage 4 - complete fracture with full displacement
'Practical' classification
Fractures best separated into intracapsular and extracapsular fractures
Intracapsular fractures reduce the blood supply to femoral head
At high risk of delayed union, non-union or avascular necrosis
If head is to be preserved they need anatomical reduction
Extracapsular fractures do not interfere with femoral head blood supply
Do not require anatomical reduction
Management
All patients require surgery if fit for an operation
Early mobilisation is associated with improved long-term prognosis
Ideally surgery should be performed within 24 hours
Postoperative rehabilitation should be by a multidisciplinary team
Intracapsular fractures
The two treatment options are:
o Reduction and internal fixation
o Femoral head replacement
Internal fixation indicated in:
o Undisplaced fractures
o Displaced fractures in young patients (<70 years)
Usually achieved with the use of three cancellous screws
Complications include non-union and avascular necrosis
Femoral head replacement indicated in:
o Displaced fractures
o Pathological fractures
Options available include:
o Cemented Thompson prosthesis
o Uncemented Austin Moore prosthesis
o Bipolar prosthesis
o Total hip replacement
Complications include dislocation, loosening and peri-prosthetic femoral fracture
Extracapsular fractures
Usually repaired with a dynamic hip screw
Allows impaction and stabilisation of fracture
Prognosis related to the number of bone fragments
90% of fractures proceed to uncomplicated fracture union
Prognosis
40% of patients with a hip fracture die within a year
50% of survivors are less independent than before the injury
Most morbidity is related to coexisting medical conditions
Bibliography
Lane J M, Russell L, Khan S N. Osteoporosis. Clin Orthop 2000; 372: 139-150.
Parker M J, Handoll H H. Conservative versus operative treatment of extracapsular
hip fractures. Cochrane Database Syst Rev 2000 (2): CD000337.
Parker M. Diagnosis and immediate care of fractured neck of femur. Hosp Med 2002;
63: 42-43.
Parker M, Johansen A. Hip fracture. BMJ 2006: 333: 27-30.
Schmidt A H, Swiontkowski M F. Femoral neck fractures. Orthop Clin North Am
2002; 33: 97-111.
Paediatric fractures
Salter and Harris classification of epiphyseal injuries
Salter and Harris fractures occur through the growth plate
Therefore they are unique to children
Classified according to degree of involvement of physis, metaphysis and epiphysis
Classification is important as it
o Determines treatment
o Determines prognosis
Type I - Epiphyseal slip - no fracture
Type II - Fracture through epiphyseal plate with proximal fragment
Type III - Fracture through epiphysis extending into the epiphyseal plate
Type IV - Fracture through both epiphysis and shaft crossing the epiphyseal plate
Type V - Crush injury causing obliteration of the growth plate
Management
In general the following statements hold true for Slater and Harris Fractures
o Type I involve growth plate but growth is rarely disturbed
o Type II fractures are the most common
o Type III fractures involve the joint and can result in chronic morbidity
o Type III fractures often require surgical treatment
o Type IV fractures can also result in chronic morbidity
o Type V fractures are difficult diagnose and can result in limb shortening
Bibliography
Patterson J M. Children's fractures 'not to be missed'. Hosp Med 2002; 63: 426-428
The knee
Anatomy
The knee joint has two component
o Articulations between the femoral and tibial condyles
o Patellofemoral joint
It is stabilised by the knee ligaments
o Anterior cruciate ligament prevents anterior translation of the tibia
o Posterior cruciate ligament prevents posterior translation if the tibia
o Medial collateral ligament provides valgus stability
o Lateral collateral ligament provides varus stability
o Posteromedial capsule resists external rotation
o Posterolateral capsule resists internal rotation
The menisci are semi-lunar shaped fibrocartilages
They increase joint congruence and distribute load across the joint
They are avascular and heal poorly beyond the peripheries
Knee movements are complex
It has dynamic stability
The joint is not a simple hinge
Clinical features
The history of any injury suggest which structure may be involved
Direct varus or valgus forces injure the collateral ligaments
Indirect forces injure the cruciate ligaments and menisci
Twisting in flexion can damage the menisci
Immediate swelling suggests a haemarthrosis
An audible 'pop' can occur with a cruciate injury
Mechanical locking is characteristic of a meniscus injury
Examination should look alignment, wasting, swelling and bruising
Localised tenderness should be elicited
The range of passive and active movement should be assessed
Provocation tests
Anterior and posterior draw test
Lachman's test
Pivot shift test
McMurray's test
Investigation
Plain radiographs may show avulsion fractures and exclude fractures around the knee
MRI is the most useful imaging modality
Shows extent of soft tissue injuries
Meniscal injuries
May be traumatic or degenerative
Classified by position and shape
Acute peripheral injuries can be repaired
Chronic central injuries often require arthroscopic partial menisectomy
Total menisectomy risk later degenerative changes and should be avoided
Anterior cruciate injuries
Acute injuries result in a haemarthrosis
Results in variable amounts of pain and instability
Often associated with medial meniscal tear
Treatment options depend on expectation and life-style of patient
Options include:
o Physiotherapy
o Early or later cruciate ligament reconstruction
The most popular grafts are:
o Hamstring graft
o Bone-patella tendon-bone graft
Posterior cruciate injuries
Usually occurs following dashboard injuries
Results in knee instability
Treatment is controversial due to less reliable surgical results
Surgical reconstruction reserved for multiple ligament injuries
Collateral ligament injuries
Medial collateral ligament injuries are more common
Clinical evaluation allows injuries to be graded
o Grade 1 - Local ligament tenderness - no instability
o Grade 2 - Unstable at 20 degrees of flexion - stable in extension
o Grade 3 - Unstable in flexion and extension
MRI is useful in evaluating extent of injury
Grade 1 injuries require analgesia and early mobilisation
Grade 2 injuries require a hinged knee brace
Grade 3 injuries require surgical repair
Bibliography
Cook J L. The current status of treatment for large meniscal defects. Clin Orth Relat Res 2005:
435: 88-95
Dowd G S. Reconstruction of the posterior cruciate ligament. Indication and results. J Bone Joint
Surg Br 2004; 86: 480-491.
Koon D, Bassett F. Anterior cruciate ligament rupture. South Med J 2004; 97: 755-756.
Smith G D, Knutson G, Richardson J B. A clinical review of cartilage repair techniques. J Bone
Joint Surg Br 2005; 87: 445-449.
The shoulder
Anterior dislocation
Shoulder is one of the commonest joints to dislocate due to:
o Shallowness of glenohumeral joint
o Range of movement
o Ligamentous laxity or glenoid dysplasia
o Vulnerability of joint
Dislocation usually caused by fall on hand
External rotation in abduction levers the head of the humerus out of the glenoid socket
Joint capsule is often torn
Glenoid labrum may be avulsed (Bankart lesion)
Clinical features
Bimodal age distribution
First peak occurs in young adult men after significant trauma
Second peak occurs in elderly women after less violence
Pain is often severe
Arm usually held in abduction and externally rotated
All movement is restricted
Lateral outline of shoulder is flattened
Bulge may be felt below clavicle
X-ray shows overlapping of humeral head and glenoid fossa
Head of humerus seen below and medial to the joint
X-ray is mandatory to exclude an humeral fracture
Treatment
Numerous methods of reduction have been described
May be reduced by simple traction / countertraction in slight abduction
Kocher's method
o Elbow flexed to 90 degrees
o Arm slowly rotated laterally to 75 degrees
o Elbow lifted forward and arm rotated medially
X-ray taken to confirm reduction and exclude fracture
Arm rested in sling for 2-3 weeks
Complications
Axillary nerve injury
Vascular injury
Fracture-dislocation
Shoulder stiffness
Unreduced dislocation
Recurrent dislocation
Posterior dislocation
Posterior dislocation is rare
Accounts for less than 2% of shoulder dislocations
Due to indirect forces resulting in internal rotation and adduction
Seen following convulsions or electric shocks
Injury is easily missed
AP x-ray may appear 'normal'
If any doubt regarding diagnosis then CT is useful
Bibliography
Cicak N. Posterior dislocation of the shoulder. J Bone Joint Surg Br 2004; 86: 324-332.
Cutts S, Prempeh M, Drew S. Anterior shoulder dislocation. Ann R Coll Surg Engl 2009; 91: 2-7
Jennings S, Cohen B. Common injuries of the shoulder. Hosp Med 2002; 63: 681-683
Peripheral nerve injuries
Neuropraxia
Temporary loss of function caused by minor trauma or pressure
Recovery occurs within minutes
Axonotmesis
Loss of function due to severe ischaemia
Recovery occurs within weeks
Neurotmesis
Loss of function due to division of nerve
No recovery occurs unless nerve is repaired
Radial nerve
Often injured in radial groove of humerus
Motor paralysis results in typical 'wrist drop' due to loss of:
o Extension of elbow, wrist, knuckles and all joints of thumb
o Supinator and brachioradialis
Sensory loss involves dorsum of 1st, 2nd and 3rd metacarpals
May be as small as the anatomical snuffbox
Picture provided by Andrew Day, Royal Sussex County Hospital, Brighton, United Kingdom
Median nerve
Often injured by penetrating wounds of the forearm
Motor paralysis due to loss of:
o The pronators
o Radial flexor of the wrist
o Flexors of all of the proximal interphalangeal joints
o Flexors of the terminal joint of the thumb, index and middle finger
o Abductor and opponens pollicis
Sensory loss over thumb, index, middle and half of ring fingers
Ulnar nerve
Often injured with fractures of the medial epicondyle of the elbow
Motor paralysis results in 'claw hand' and hypothenar wasting due to loss of:
o Ulnar flexor of the wrist
o Flexors of the terminal phalanx of the ring and little finger
o Muscles of the hypothenar eminence
o Adductor pollicis
o Palmar brevis
All the interossei and the medial two lumbricals
Sensory loss over little and half of ring finger
Picture provided by Loh Yin, International Medical University, Jolam Rasah. Malaysia
Picture provided by Alan Parbhoo, Barts and Royal London Hospital, United Kingdom
Brachial plexus injuries
Usually occur in two situations
o Difficult vaginal deliveries associated with the use of forceps
o Traction during a fall or road traffic accident
Erb's palsy
Due to damage to the upper nerve roots
Usually involves C5, C6, C7
Abductors and external rotators of the shoulder are affected
Loss of finger extension
Sensation is intact
Klumpke's palsy
Due to damage to the lower nerve roots
Usually involves C8, T1
All finger muscles are paralysed
Loss of sensation
Often associated with unilateral Horner's syndrome
Bibliography
Leffert R D. Nerve lesions about the shoulder. Orthop Clin North Am 2000; 31: 331-345.
Terzis J K, Vekris M D, Soucacos P N. Brachial plexus root avulsions. World J Surg 2001; 25:
1049-1061
Upper limb disorders
Painful shoulder
Anatomy
Shoulder joint is made up of a complex of five joints
o Sternoclavicular joint
o Acromioclavicular joint
o Subacromial space
o Glenohumeral joint
o Scapulothoracic joint
Glenohumeral joint is stabilised by a number of muscles
These include deltoid muscle and the rotator cuff muscles
The rotator cuff is made up of:
o Supraspinatus
o Infraspinatus
o Teres minor
o Subscapularis
Clinical features
Causes of shoulder pain include
o Impingement syndromes
o Rotator cuff tears
o Frozen shoulder
o Calcific tendonitis
Rotator cuff impingement
Due to abrasion of rotator cuff muscles on coracoacromial arch
Impingement is usually reversible
May lead to rotator cuff tears or degenerative changes in glenohumeral joint
Causes a painful arc between 60 and 120 degrees of abduction
Full range of passive movement is possible
Plain radiographs may be normal
Treatment included
o Subacromial steroid injection
o Subacromial decompression
Rotator cuff tears
Usually occur in middle age and elderly
Result from either chronic impingement or acute injury
Usually present with pain and weakness
Supraspinatus and Infraspinatus are usually involved
Result in weakness if abduction and resisted external rotation
US or MRI should be obtained to:
o Confirm the clinical diagnosis
o Assess the size of the tear
o Assess the extent of retraction
Treatment options include
o Conservative management
o Open or arthroscopic repair
Frozen shoulder
Due to chronic inflammation and fibrosis of subsynovial layer
Often occurs after minor trauma or period of immobility
Reduces range of active and passive movement, particularly loss of external rotation
Associated with severe pain
Recovery may be prolonged
Treatment options include
o NSAIDs
o Physiotherapy
o Manipulation under anaesthetic
Calcific tendonitis
Due to deposition of calcium salts in supraspinatus tendon
Produces severe pain over anterolateral aspect of shoulder
Full range of passive movement
Pain is aggravated by shoulder movement
Calcium deposits on x-ray are diagnostic
Treatment options include
o NSAIDs
o Physiotherapy
o Subacromial injection
o Subacromial decompression and removal of calcium deposits
Lateral epicondylitis
Often referred to as tennis elbow
Due to inflammation at the origin of the wrist and finger extensors
Its is an enthesopathy of the lateral epicondyle
Clinical features
Occurs between 30 and 50 years of age
Men and women are equally affected
75% experience symptoms in their dominant arm
Causes pain over the lateral epicondyle radiating to the forearm
Tenderness is usually maximum 5 mm distal to the insertion of the tendon
Resisted wrist extension increases the pain
Plain x-ray may show calcification in the soft tissues
Management
Non surgical management involves
o Rest
o Non-steroidal anti-inflammatory medication
o Steroid injection
Surgical treatment if no improvement with 6 months conservative treatment
Involves division and reattachment of the tendon
85% notice a dramatic improvement in symptoms
Medial epicondylitis
Often referred to as golfer's elbow
It is less common than lateral epicondylitis
Occurs in same age group
is is an enthesopathy of the pronator teres and flexor carpi radialis tendon
Characterised by pain over the medial aspect of the elbow
Pain is exacerbated by wrist flexion
Tenderness is distal to medial epicondyle
Management is similar to lateral epicondylitis
Ulnar nerve entrapment at the elbow
Ulnar nerve runs behind medial epicondyle at the elbow
Runs in a tunnel formed by aponeurosis between tow head of flexor carpi ulnaris
Aponeurosis is slack in elbow extension
Becomes tight in elbow flexion
Disorders of the elbow joint can result in nerve compression
Symptoms are often worse when elbow is flexed
Clinical features
Pain and paraesthesia in the ring and little finger
Weakness of grasp and grip
Loss of manual dexterity
Wasting of the intrinsic muscles of the hand
Management
Night splints to reduce elbow flexion may improve symptoms
Surgical options include
o Ulnar nerve decompression
o Medial epicondylectomy
o Anterior transposition
Bibliography
Buchbinder R, Green S, Bell S et al. Surgery for lateral elbow pain. Cochrane Database Syst Rev
2002; CD003524.
Green S, Buchbinder R, Barnsley L et al. Non-steroidal anti-inflammatory drugs (NSAIDs) for
treating lateral elbow pain in adults. Cochrane Database Syst Rev 2002; CD003686.
Smidt N, Assendelft W J, van der Windt D A et al. Corticosteroids for lateral epicondylitis: a
systemic review. Pain 2002: 96: 23-40.
Common disorders of the hand
Carpal tunnel syndrome
Carpal tunnel formed by flexor retinaculum stretching across carpus
Forms a tight tunnel through which passes
o Long flexors to fingers and thumb
o Median nerve
Swelling within the tunnel causes nerve compression and ischaemia
Carpal tunnel syndrome affects 3% of women and 2% of men
30% cases due to underlying medical condition
Causes
Idiopathic
Hormonal - pregnancy / menopause
Rheumatoid arthritis
Hypothyroidism
Diabetes
Clinical features
Usually presents in middle age
Female : male ratio is 8:1
Pain and paraesthesia in distribution of median nerve
Symptoms are often worse at night
Signs are few
Tapping over carpal tunnel can reproduce symptoms (Tinel's sign)
Flexion of wrist for 60 seconds reproduces symptoms (Phalen's sign)
Thenar wasting and loss of 2-point discrimination are late features
Diagnosis confirmed by electomyelogram
Shows slowed nerve conduction across the wrist
Management
Treat underlying associated medical problems
Nocturnal symptoms can often be controlled with night splints
Steroid injections may produce temporary symptomatic relief
Troublesome symptoms require division of flexor retinaculum
May be performed endoscopically
70-90% are symptom-free following surgery
de Quervain's disease
Also known as stenosing tenovaginitis
Due to inflammation and thickening of tendon sheaths of
o Extensor pollicis brevis
o Abductor pollicis longus
Occurs where both tendons cross the distal radius
Clinical features
Usually presents in middle age
Pain noted over radial aspect of wrist
Often occurs after repetitive activity
Tendon sheath is thickened and tender over the radial styloid
Pain often worsened by abduction of thumb against resistance
Passive abduction across palm often causes pain (=Finkelstein's test)
Management
Symptoms can often be improved with steroid injections into tendon sheath
Persistent symptoms require surgery
Tendon sheath should be split avoiding the dorsal sensory branch of radial nerve
Dupuytren's contracture
Fibroproliferative disease of the palmar fascia
First described in 1614
Detailed anatomical study presented by Dupuytren in 1831
Aetiology unclear
Possibly inherited as an autosomal dominant condition with limited penetrance
Occasionally associated with plantar fasciitis and Peyronie's disease
More common in northern Europe
Male to female ratio 4:1
Affects 5% men older than 50 years
Clinical features
Thickening of palmar fascia with nodule formation
Flexion contracture at MCPJ and PIPJ
Usually affects ring and little finger
In late stage of the disease cords develop proximal to the nodules
65% cases are bilateral
Risk factors
Diabetes mellitus
Alcohol excess
HIV infection
Epilepsy
Trauma
Manual labour
Management
Excision or incision of the palmar fascia
Options include fasciotomy, fasciectomy or dermofasciectomy
Consider surgery if:
o MCP contracture is greater than 30 degrees
o There is functional disability
Need intensive postoperative physiotherapy
Approximately 20% patients develop complications
Recurrence rate is approximately 50%
Ganglions
Commonest cause of swellings around the hand and wrist
Cystic lesions arising from either the joint capsule of tendon sheath
Aetiology is unknown
More common in women
Usually occur between 20 and 40 yrs of age
70% of ganglions occur around the wrist
Clinical features
Most present as smooth swellings 2-4 cm in diameter
Most are painless
Pain can occur due to compression of adjacent neurovascular structures
Management
If ganglion is asymptomatic no specific treatment is required
The hold treatment of 'hitting with the family bible' should be condemned
Aspiration can be attempted but outcome is poor
Excision is the treatment of choice
Lesion should be explored down to joint capsule or tendon sheath
Inadequate surgery results in a high recurrence rate
Bibliography
England J D. Entrapment neuropathies. Cur Opin Neurol 1999; 12: 597-602.
Frank P L. An update on Dupuytren's contracture. Hosp Med 2001; 62: 6780681.
Gerritsen A A M, Uitehaag B M J, van Geldere D, Scholten R J P M, de Vet H C W, Bouter L
M. Systematic review of randomised clinical trials of surgical treatment for carpal tunnel syndrome.
Br J Surg 2001; 88: 1285-1295.
Gudmundsson K G, Jonsson T, Amgrimsson R. Guillamme Dupuytren and finger contractures.
Lancet 2003; 362: 165-168.
Hart M G, Hooper G. Clinical association of Dupuytren's disease. Postgrad Med J 2005; 81: 425-
428.
Katz J N, Simmons B P. Carpel tunnel syndrome. New Eng J Med 2002; 346: 1807-1812.
Kloen P. New insights in the development of Dupuytren's contracture: a review. Br J Plast Surg
1999; 52: 629-635.
Marshall S, Tardif G, Ashworth N. Local corticosteroid injection for carpal tunnel syndrome.
Cochrane Database Syst Rev 2000: 4: CD001554.
Preston D C. Distal median neuropathies. Neurol Clin 1999; 17: 407-424.
Saar J D, Grothaus P C. Dupuytren's disease: an overview. Plast Reconstr Surg 2000; 106: 125-
134
Sen D, Chhaya S, Morris V H. Carpel tunnel syndrome. Hosp Med 2002; 63: 392-395.
Stenback G. The carpal tunnel syndrome. J Emerg Med 1999; 17: 519-253.
Tennent T D, Goddard N J. Carpal tunnel decompression: open vs. endoscopic. Br J Hosp Med
1997; 58: 551-554.
Thornburg L E. Ganglions of the hand and wrist. J Am Acad Orthop Surg 1999; 7: 231-238.
Thurston A J. Dupuytren's disease. J Bone Joint Surg [Br] 2003; 85: 496-505.
Lower limb disorders
Achilles tendon rupture
Anatomy
Achilles tendon formed from combined tendons of soleus and gastrocnemius
Approximately 15 cm in length
Often transmits forces ten time body weight
Tendon is enclosed with a paratenon rather than synovial sheath
Blood supply is tenuous 3-6 cm proximal to calcaneal insertion
Pathology
Rupture usually occurs in fit, active men
Commonest age is 20 to 40 years
Rupture occurs within tendon
Usually occurs 3-4 cm proximal to insertion
Rupture is usually caused by sudden force to dorsiflexed foot
Picture provided by J M Gauer, Kantonsspital Schaffhausen, Switzerland
Clinical features
Usually no preceding pain or history of trauma
Presents with snapping sensation
Followed by acute pain over the tendon
Plantar flexion of the foot is reduced
Often a gap is palpable at the site of the rupture
With the patient prone, plantar flexion on calf compression is abolished (Thompson's test)
Management
Aim is to restore continuity of the tendon
Can be achieved with surgical or non-operative approaches
Surgery is probably more appropriate in fit, active individuals
Non-operative management is probably more appropriate in elderly or unfit
Surgery
Can be performed by either an open or percutaneous technique
During open surgery
o Incision is made over the tendon
o Paratenon is opened
o Ends of tendon are apposed using a non-absorbable suture
o Repair performed using either a Kessler or Bunnell Technique
o Paratenon is closed over repair
Same can be achieved using a percutaneous technique
Patient requires an equinus splint for 2 weeks
The ankle is then gradually dorsiflexed
Re-rupture rate is less than 5%
Picture provided by J M Gauer, Kantonsspital Schaffhausen, Switzerland
Non-operative approach
Patient is maintained in short-leg equinus cast for at least 6 weeks
Re-rupture rate as high as 40% have been recorded
Bibliography
Coull R, Williams R L. Common injuries of the foot and ankle. Hosp Med 2002; 63: 624-625.
McClelland D, Maffulli N. Percutaneous repair of ruptured Achilles tendon. J R Coll Surg Ed
2002; 47: 613-618.
Maffulli N. Rupture of the Achilles tendon. J Bone Joint Surg Am 1999; 81: 1019-1036.
Common problems of the foot
Hallux valgus
Commonest deformity of the foot
Results in excessive valgus angulation of the big toe
Only seen in populations that wear shoes
Splaying of the forefoot with varus angulation of the first metatarsal predisposes
The anatomical deformity consists of:
o Increased forefoot width
o Lateral deviation of the hallux
o Prominence of the first metatarsal head
As deformity increases long tendons of the hallux are shifted laterally
Clinical features
More common in women
Often bilateral
Symptoms result from
o A bursa over metatarsal head = bunion
o Hammer toes
o Metatarsalgia
o Osteoarthritis of the first MTPJ
Diagnosis can be confirmed on x-ray
Intermetatarsal angle should be less than 20 degrees
Hallux angle should be less than 15 degrees
Picture provided by Ronan Caspi, Tel Aviv, Israel
Management
Surgical management should be considered if patient is symptomatic
Options include:
o First metatarsal osteotomy
o Exostectomy and capsulorraphy
o Excision of proximal one-third of proximal phalanx (Keller operation)
o Arthrodesis
Hallux rigidus
Due to osteoarthritis of first MTPJ
Affects men more often than women
Results in pain on walking, especially on rough ground
There is no valgus deviation of the hallux
MTPJ is swollen and enlarged
Dorsiflexion of the MTPJ is reduced
A rocker-soled shoe may improve symptoms
If significant symptoms occur then surgery may be required
Options include:
o Extension osteotomy
o Cheilectomy
o Arthroplasty
o Arthrodesis
Claw toes
Results from:
o Flexion of the interphalangeal joints
o Hyperextension of the metatarsophalangeal joints
Often idiopathic
Can be associated with:
o Rheumatoid arthritis
o Poliomyelitis
o Peroneal muscular atrophy
Clinical features
Pain in the forefoot = metatarsalgia
Symptoms are usually bilateral
Walking may be restricted
Painful callosities on the dorsum of the toes or under the metatarsal heads
Picture provided by Ronan Caspi, Tel Aviv, Israel
Management
If the toes can be passively straightened than a 'metatarsal bar' may help
Special footwear may reduce symptoms
If non-operative management fails then surgical options include
o Interphalangeal arthrodesis
o Joint excision
o Metatarsal osteotomy
o Digital amputation
Plantar fasciitis
Self-limiting condition that occurs in middle age
Presents with intermittent inferior heal pain
Usually unilateral but 15% cases are bilateral
Pain often worse early in the morning
Examination show tenderness over the medial plantar aspect of the calcaneal tuberosity
50% have heel spur on plain x-ray
Differential diagnosis includes:
o Reiter's syndrome
o Entrapment neuropathy
o Calcaneal stress fracture
Management should involve the use of
o Supportive heel pads and other orthotic devices
o Non-steroidal anti-inflammatory drugs
Surgery is rarely indicated
Morton's neuroma
Painful forefoot disorder
Caused by thickening and fibrosis of interdigital nerves
Aetiology is unknown
Usually affects second or third web space
Causes plantar pain at level of metatarsal heads
May be associated with distal sensory loss
Differential diagnosis includes
o Metatarsalgia
o Metatarsophalangeal synovitis
o Stress fracture
o Frieberg's infarction
Initial management is non-operative
Surgical excision of the neuroma should be considered if symptoms fail to settle
Bibliography
Coughlin M J. Hallux valgus. J Bone Joint Surg Am 1996; 78; 932-936
Ferrari J, Higgins J P, Williams R L. Interventions for treating hallux valgus (abductovalgus) and
bunions. Cochrane Database Syst Rev 2000; CD000964.
Singh S K, Loli J P, Chiodo C P. The surgical treatment of Morton's neuroma. Current
Orthopaedics 2005: 19: 379-384
Degenerative and rheumatoid arthritis
Osteoarthritis
Osteoarthritis is the commonest condition affecting synovial joints
No longer considered simple joint 'wear and tear'
Change in cartilaginous matrix is probably important
Primary OA is of unknown aetiology
Secondary OA is the result of congenital, infective joint disorders or trauma
Pathology characterised by:
o Loss of hyaline cartilage
o Subchondral bone sclerosis
o Subchondral cyst formation
o Osteophyte formation
Several patterns of joint involvement recognised including:
o Generalised nodular OA
o Large joint osteoarthritis
Clinical features
Joint pain - worse after exercise or at end of day
Pain relieved by rest
Limited early morning stiffness
Limited stiffness after rest
Bony joint swelling
Few systemic features
Management
Aims of treatment are to:
o Reduce joint pain
o Improve joint function
In early stages pain can often be improved with simple analgesia
Life style modification is also important
NSAIDs can often help
Intra-articular steroids can reduce symptoms
If fails to improve with conservative measures surgery may be required
Surgical options for degenerative joints are
o Arthroscopic lavage and debridement
o Osteotomy - alteration of joint alignment
o Arthroplasty - replacement of diseased joint
o Arthrodesis - fusion of disease joint
Rheumatoid arthritis
Rheumatoid arthritis is an autoimmune inflammatory synovial disease
Aetiology if unknown
Worldwide prevalence is approximately 1%
Female : male ratio is 3:1
Onset most often seen between 20 and 40 years
Usually symmetrically affects multiple joints
Commonest joints affected are hand, elbow, knee and cervical spine
Also affects synovium of tendon sheaths
Often part of a systemic inflammatory process
More common in those with HLA DR4 and DW4
Pathologically characterised by:
o An inflammatory process within the synovium
o Joint destruction and pannus formation
o Periarticular erosions
Clinical features
Joint pain - worse during exercise
Pain relieved by movement
Prolonged early morning stiffness
Prolonged stiffness after rest
Marked soft tissue swelling and erythema
Systemic features often present
Extra-articular manifestations
Occur in approximately 20% of patients
Ocular
o Keratoconjunctivitis sicca
o Episcleritis
o Scleritis
Pulmonary
o Pulmonary nodules
o Pleural effusion
o Fibrosing alveolitis
Cardiac
o Pericarditis / pericardial effusion
o Valvular heart disease
o Conduction defects
Cutaneous
o Palmar erythema
o Rheumatoid nodules
o Pyoderma gangrenosum
o Vasculitic rashes and leg ulceration
Neurological
o Nerve entrapment
o Cervical myelopathy
o Peripheral neuropathy
o Mononeuritis multiplex
Management
Requires a multidisciplinary approach
Disease modifying drugs include:
o NSAIDs
o Methotrexate, sulphasalazine, penicillamine, gold
o Corticosteroids
o Cytotoxic drugs
Specific syndromes
Several syndromes have been described associated with rheumatoid arthritis
Felty's syndrome
o Rheumatoid arthritis
o Neutropenia
o Lymphadenopathy
o Splenomegaly
Still's disease
o Rheumatoid arthritis in childhood
o Rash
o Fever
o Splenomegaly
Sjogren's syndrome
o Rheumatoid arthritis
o Reduced lacrimal and salivary secretion
Bibliography
Grainger R, Cicuttini F M. Medical management of osteoarthritis of the knee and hip. Med J Aust
2004; 180: 232-236.
Gupta K B, Duryea J, Weissmann B N. Radiographic evaluation of osteoarthritis. Radiol Clin
North Am 2004; 42: 1-9.
Haq I, Murphy E, Dacre G. Osteoarthritis. Postgrad Med J 2003; 79: 377-383.
Hunter D J, Felson D T. Osteoarthritis. BMJ 2006; 332: 639-342
Scott D L. Advances in the medical management of rheumatoid arthritis. Hosp Med 2002: 63:
294-297.
Walker-Bone K, Javaid K, Arden N, Cooper C. Medical management of osteoarthritis. Br Med J
2000; 321: 936-940.
Osteoporosis
Osteoporosis is a systemic skeletal disease characterised by:
o Low bone mass
o Micro-architectural deterioration
It is associated with increased bone fragility and susceptibility to fractures
It is defined as a bone mineral density less than 2.5 standard deviations below the mean
Established osteoporosis is a low bone mineral density associated with an osteoporosis-related
fracture
Pathophysiology
Bone undergoes continuous resorption and formation
10% of adult skeleton is remodelled each year
Bone loss results from an imbalance between resorption and formation
Human skeleton comprises approximately
o 80% cortical bone
o 20% trabecular bone
Osteoporotic fractures occur at sites with more than 50% trabecular bone
o Vertebral body
o Proximal femur
o Distal forearm
Bone loss leads to thinning of the trabecular plates
This causes a disproportionate loss of bone strength
Peak bone mass is achieved by the age of 30 years
After skeletal maturity bone is lost at about 1% per year
Women experience accelerated bone loss after the menopause
Factors associated with increased bone loss include:
o Inactivity
o Cigarette smoking
o Poor diet
o Family history
o Early menopause
o Endocrine disease - Cushing's syndrome, diabetes, hyperthyroidism
o Drugs - Steroids, thyroxine, diuretics
Clinical features
Osteoporosis-related fractures
Increased mortality
Pain
Deformity
Loss of independence
Investigation
Radiology
Dual-energy x-ray absorptionometry
Quantitative CT scanning
Quantitative ultrasound
Bone biopsy
Biochemical markers of bone turnover
Prevention
Optimisation of peak bone mass
o Exercise
o Dietary calcium
Reduce rate of bone loss
o Hormonal replacement therapy
o Moderate alcohol intake
o Stop smoking
Bibliography
Christodoulou C. Cooper C. What is osteoporosis? Postgrad Med J 2003; 79: 133-138.
Compston J. Prevention and treatment of osteoporosis. Clinical guideline and new evidence. J R
Coll Physicians Lond 2000; 34: 518-521.
Eastell R. Treatment of postmenopausal osteoporosis. N Engl J Med 1998; 338: 736-746.
Kanis J A. Diagnosis of osteoporosis and assessment of fracture risk. Lancet 2002; 359: 1929-
1936.
Theodorou S J, Theodorou D J, Sartoris D J. Osteoporosis and fractures; the size of the problem.
Hosp Med 2003; 64: 87-9.
Metabolic bone disease
Bone is composed of both cells and matrix
Also contains blood vessels, nerves and haemopoeitic system
Bones cells
o Osteoblasts are responsible for bone formation
o Osteoclasts are responsible for bone resorption
o Serum alkaline phosphatase reflects osteoblastic activity
Matrix
o Has both mineralised and unmineralised components
o Mineralised component is made up of hydroxyapatite
o Osteoid is the unmineralised component
o Made up of 90% collagen and 10% non-collagenous proteins
o Non-collagenous proteins include proteoglycans and glycoproteins
Calcium homeostasis
98% of bodies calcium is stored within the skeleton
At homeostasis turnover results in equal flux in and out of skeleton
Calcium homeostasis is maintained by parathyroid hormone, Vitamin D3 and calcitonin
Parathyroid hormone
84 amino acid protein produced by parathyroid glands
Increases serum calcium
Increases renal calcium reabsorption
Increases skeletal turnover
Increases renal production of dihydroxy-vitamin D3
Cholecalciferol
Is vitamin D3
Under normal circumstances is produced in the skin by action of sunlight on precursors
Hydroxylated in the liver to 25-hydroxy-vitamin D3
Hydroxylated in kidney to 1,25 dihydroxy-vitamin D3
Increases renal reabsorption of calcium
Increases gastrointestinal absorption of calcium
Increases skeletal calcium resorption
Calcitonin
Produced by thyroid parafollicular C cells
Reduces serum calcium
Inhibits bone calcium resorption
Osteomalacia and rickets
Vitamin D deficiency results in incomplete osteoid mineralisation
In childhood, prior to epiphyseal closure, causes rickets
In adults causes osteomalacia
Causes
Vitamin D deficiency
o Malabsorption
o Post-gastrectomy or bowel resection
o Coeliac disease
Cirrhosis
Renal disease
o Renal tubular disorder (e.g. familial hypophosphataemic rickets)
o Chronic renal failure
Anticonvulsant therapy
Tumours
Clinical features
Osteomalacia usually due to dietary deficiency in the elderly or Asian population
Rickets usually due to familial hypophosphataemic rickets
Rickets usually presents in early childhood with
o Failure to thrive
o Valgus or varus long bone deformities
o Skull deformities = craniotabes
o Enlarged costochondral junctions = Rickety rosary
o Lateral indentation of the chest wall = Harrison's sulcus
o X-ray shows widened epiphyses and cupped distal metaphysis
Osteomalacia presents with
o Bone pain and tenderness
o Proximal myopathy
o True pathological or pseudo-fractures
o X-ray shows translucent bands in medical femoral cortex, pubic ramus or scapula
o = Looser's zones
In osteomalacia
o Serum calcium and phosphate are low
o Alkaline phosphatase is increased
In familial hypophosphataemic rickets
o Serum calcium is normal and phosphate is low
Bone biopsy would show increased unmineralised osteoid
Treatment
Vitamin D replacement therapy
Phosphate supplements in familial hypophosphataemic rickets
Bibliography
Renton P. Radiology of rickets, osteomalacia and hyperparathyroidism. Hosp Med 1998; 59: 399-
403.
Paget's disease of bone
Named after Sir James Paget (1814-1899)
First described osteitis deformans in 1877
Aetiology is unknown - possibly due to a viral infection
Often an incidental finding on x-ray in an asymptomatic patient
If symptomatic usually causes bone pain
Clinical signs include characteristic skull and long bone deformities
Complications
Pathological fractures - complete or incomplete
Neurological effects
o Cranial nerve lesions
o Spinal cord lesions
Osteoarthritis
Sarcomas
Cardiac failure
Histological features
Osteoclasts are enlarged
Increased bone turnover produces a mosaic pattern of lamellar bone
Three phases recognised - osteolytic, mixed and sclerotic
Radiological features
Osteolytic phase can produce osteoporosis circumscripta
Bone softening can produce bowing, platybasia, protrusion acetabuli or greenstick fractures
Mixed phase shows generalised bone enlargement
Sclerotic phase shows increased density, trabeculae and cortical thickening
Biochemistry
Serum calcium and phosphate are usually normal
Serum alkaline phosphatase is increased
Uric acid increased in about 30% of patients
Treatment
Non-steroidal anti-inflammatory agents will control bone pain
Biphosphonates will reduced bone turnover
Neurological complications and fractures may require surgical intervention
Paget's sarcomas
Most osteosarcomas that develop lat in life are associated with Paget's disease
Malignant change occurs in less than 1% patients with Paget's disease
50% are osteosarcomas
25% are fibrosarcomas
25% are giant-cell sarcomas
The commonest site is the femur
Prognosis of Paget's sarcomas is poor
Median survival is one year
Only 5% alive at five years
Bibliography
Keen R W. The current status of Paget's disease of bone. Hosp Med 2003; 64: 230-232.
Ooi C G, Fraser W D. Paget's disease of bone. Postgrad Med J 1997; 73: 69-74.
Hip replacement surgery
Operation developed by Sir John Charnley in 1960s
More than 50,000 hip replacements are performed each year in United Kingdom
Over one million hips have been replaced worldwide
Over 100 different types of prosthesis have been used
The 'gold standard' is the Charnley cemented prosthesis
Principle components
Acetabular component
Usually made of high density polyethylene
Biocompatible, low coefficient of friction, low rate of wear
Ceramic acetabular component have improved surface properties
Are expensive and have tendency to brittle failure
Metal cups are obsolete due to high friction, loosening and wear
Femoral component
Usually made of stainless steel, titanium or cobalt chrome alloy
Resistant to corrosion with high endurance
Improved longevity seen with small femoral head
Polymethylmethacrylate cement
Acts as a filling agent without adhesive properties
Macrolocking occurs with cement in drilled holes
Microlocking occurs with cement in interstices of cancellous bone
Produces an exothermic reaction during preparation
Addition of barium weakens the cement
Antibiotic impregnation may increase resistance to infection
Recently uncemented prostheses have been developed
Require more exacting insertion technique
Anchored by interference fit achieved by porous surface or hydroxyapatite coating
Uncemented prostheses have a tendency early failure
Indications
Osteoarthritis
Rheumatoid arthritis
Still's disease
Ankylosing spondylitis
Congenital dysplastic or dislocated hips
Paget's disease
Trauma or avascular necrosis
Septic arthritis
Contraindications
Uncontrolled medical problems
Skeletal immaturity
Active infection
Neuropathic joint
Progressive neurological disease
Muscle weakness
Aims of surgery
Patients should have significant pain, functional disturbance and failed conservative therapy
The principle aims of surgery are:
o To reduce joint pain
o Improve joint function
Operative technique
Avoid operation in patients with a septic focus
Thorough skin preparation with sterile adhesive plastic drapes
Operating team should wear two pairs of gloves
Body exhaust suites may be worn
Laminar air flow should be provided in operative field
Antibiotic prophylaxis should be given
Specific complications
Neurovascular injuries
Leg length discrepancy
Dislocation
Infection
Aseptic loosening
Implant wear and failure
Heterotopic ossification
Femoral fractures
Trochanteric non-union
Abductor mechanism weakness
Outcome
Outcome is affected by many factors including
o Type of implant used
o Underlying diagnosis
o Sex of patient
o Cement type
o Cementing technique
o Surgical approach
Joint resurfacing
Outcome of joint replacement surgery in less predictable in
o Younger patients
o Those with active life style
Metal on metal hip resurfacing developed for use in younger patients
Head of femur preserved which is developed into chamfered cylinder
Metal head is cemented in place
Metal cup is placed in acetabulum
Compared to THR, has lower risk of complications
o Lower risk of dislocation
o Less bone loss
o Lower risk of component loosing
Short-term results are very encouraging
Long-term outcome unclear
Bibliography
Clarke I C, Donaldson T, Bowsher J G et al. Current concepts of metal-on-metal hip resurfacing.
Orth Clin North Am 2005; 36: 143-162.
Grigoris P, Roberts P, Pabousis K et al. The evolution of hip resurfacing arthroplasty. Orth Clin
North Am 2005; 36: 125-134.
Latham J, Treacy R B C, Shetty V D, Villar R N. To resurface or replace the hip in the under 65-
year old. Ann R Coll Surg Engl 2006; 88: 349-353
Salah K J, Kassim R, Yoon P, Vorlicky L N. Complications of total hip arthroplasty. Am J Orthop
2002; 31: 485-488.
Infected joint replacement
Over 100,000 knee and hip replacements are performed in the UK each year
Most are carried out with few complications
Infections is an uncommon but devastating complication
Occurs in approximately 1% cases
Results in major morbidity and considerable cost
Risk can be reduced by:
o Excluding patients who have active infection
o Antibiotic prophylaxis
o Careful theatre technique
Microbiology
Commonest organisms identified are:
o Coagulase-negative staphylococcus (45%)
o Staph. aureus (35%)
o Streptococci (10%)
o Gram-negative bacteria (<5%)
Early infection results form intraoperative contamination
Late infection usually results from haematogenous spread
Bacteria adhere to prosthetic material and produce a biofilm
Biofilm isolates the bacteria from host defences and antibiotics
Significant infection can result from small bacterial inoculum
A low-grade inflammatory process then occurs
This leads to bone erosion and loss of bone stock
Clinical features
Acute infection presents with sign of a wound infection
A purulent discharge from the wound is often present
Chronic infection presents more insidiously
Pain is often the prominent symptom
The diagnosis of chronic infection can be difficult
Investigation
The following investigations should be considered
o Microbial culture
o Inflammatory markers
o Plain radiography
o Bone scan
o Histology
o Molecular methods
Diagnosis depend on identification of bacteria from fluid around joint
Management
Antibiotics should be started once diagnosis is considered
Rarely eradicate establish infection
Antibiotic choice should be based on culture results
If cultures are negative or unavailable then vancomycin is the organism of choice
Surgery
In acute infection joint debridement and washout may be appropriate
In chronic infection with a loose joint, implant should be removed
Revision surgery can be performed as a one-stage or two-stage procedure
If insertion of new prosthesis is impossible consider:
o Excision arthroplasty
o Joint fusion
Complications following revision joint surgery include:
o Massive bone loss
o Periprosthetic fracture
o Recurrence of infection
Bibliography
Gillespie W J. prevention and management of infection after total joint replacement. Clin Infect Dis
1997; 25: 1310-1317.
Nelson C L. Primary and delayed exchange for infected total knee arthroplasty. Am J Knee Surg
2001: 14; 60-64.
Kaltas D S. Infection after total hips arthroplasty. Ann R Coll Surg Engl 2004; 86: 267-271.
Acute osteomyelitis
Acute osteomyelitis usually occurs in children
Usually a haematogenous infection from distant focus
Organisms responsible include:
o Staph. aureus
o Strep. pyogenes
o H. influenzae
o Gram-negative organisms
Salmonella infections are often seen in those with sickle-cell anaemia
Infection usually occurs in metaphysis of long bones
Pathology
Acute inflammation results in raised intraosseous pressure and intravascular thrombosis
Suppuration produces a subperiosteal abscess that may discharge into soft tissues
Spread of infection into epiphysis can result in joint infection
Within days bone death can occur
Fragments of dead bone become separated in medullary canal (sequestrum)
New bone forms below stripped periosteum (involucrum)
If infection rapidly controlled resolution can occur
If infection poorly controlled chronic osteomyelitis can develop
Clinical features
Child usually presents with pain, malaise and fever
Often unable to weight bear
Early signs of inflammation are often few
Bone is often exquisitely tender with reduced joint movement
Late infection presents with soft-tissue swellings or discharging sinus
Diagnosis can be confirmed by aspiration of pus from abscess or metaphysis
50% of patients have positive blood cultures
Radiology
X-rays can be normal during first 3 to 5 days
In the second week radiological signs include:
o Periosteal new bone formation
o Patchy rarefaction of metaphysis
o Metaphyseal bone destruction
In cases of diagnostic doubt bone scanning can be helpful
Differential diagnosis
Cellulitis
Acute suppurative arthritis
Rheumatic fever
Sickle-cell crisis
Management
General supportive measures should include intravenous fluids and analgesia
Painful limb often requires a splint of skin traction to relieve symptoms
Aggressive antibiotic therapy should be instituted
Flucloxacillin is often the antibiotic of choice
If fails to respond to conservative treatment surgery may be required
A subperiosteal abscess should be drained
Drilling of metaphysis is occasionally required
Overall, about 50% of children require surgery
Complications
Metastatic infection can occurs at distant sites (e.g. brain, lung)
Spread into joint can result in a septic arthritis
This complication occurs in:
o Young children in whom the growth plate is permeable
o Bones in which the metaphysis is intracapsular
o Epiphysis of bones involved in metastatic infection
Involvement of physis can result in altered bone growth
Failure to eradicate infection can result in chronic osteomyelitis
Bibliography
Berendt T, Byren I. Bone and joint infection. Clin Med 2004; 4: 510-518
Frank G, Mahoney H M, Eppes S C. Musculoskeletal infections in children. Pediatr Clin North
Am 2005; 52: 1083-1106.
Lazzarini L, Mader J T, Calhoun J H. Osteomyelitis in long bones. J Bone Joint Surg Am 2004;
38: 1855-1859.
Lew D P, Waldvogel F A. Osteomyelitis. Lancet 2004; 364: 369-379.
Ray P S, Simonis R B. Management of acute and chronic osteomyelitis. Hosp Med 2002; 63: 401-
407.
Parsons B, Strauss E. Surgical management of chronic osteomyelitis. Am J Surg 2004; 188 (Suppl
1): 57-66
Septic arthritis
Acute inflammatory condition of a joint
Usually results from bacterial infection
Untreated it will lead to destruction of the articular cartilage
50% cases occur in children less than 3 years of age
In infants less than one year old the hip is the commonest joint involved
In older children the knee is the commonest joint affected
10% of patients have multiple joints involved
Microbiology
Infecting organism depends on age
Children Adults
< 3 years old > 3 years old < 50 years old > 50 years old
H. influenzae Staph aureus Staph aureus Staph aureus
Staph aureus H. influenzae Neisseria gonorrhoea Gram-negative
Coliforms Streptococci
Organism can enter joint via a number of routes
o Penetrating wound
o From epiphysis or metaphysis
o Haematogenous spread
Provoke an acute inflammatory response
Large number of neutrophils accumulate in joint
Release proteolytic enzymes that break down the articular cartilage
Results in joint effusion and reduced synovial blood supply
Complications of septic arthritis include
o Avascular necrosis of epiphysis
o Joint subluxation / dislocation
o Growth disturbance
o Secondary osteoarthritis
o Persistent or recurrent infection
Clinical features
Exact presentation depends on age
Children are usually systemically unwell
Present with pain in the affected joint
All movements of the joint are painful
Reluctant to stand on weight-bearing joints
Affected joint is usually swollen, red and warm
Hip involvement results in flexion and external rotation
In adults septic arthritis is usually associated with immunosuppression
Picture provided by Mohamed Atanis, El Wafa Clinic, Al Marj, Libya
Investigations
Key investigation is culture of a joint aspirate
Should be performed prior to the administration of antibiotics
Other appropriate investigations should include
o Inflammatory markers
o Plain x-rays
o Bone scan
Differential diagnosis
Irritable hip
Perthe's disease
Osteomyelitis
Gout
Pseudogout
Management
Antibiotics should be started after joint aspiration
Empirical therapy should be commenced based on likely organisms
Adjusted depending antibiotic sensitivity
Antibiotics should be continued for 6 weeks
Surgery
Involves joint drainage and lavage
May be performed arthroscopically
Early joint mobilisation should be encouraged
Bibliography
Garcia De la Torre I. Advances in the management of septic arthritis. Rheum Dis Clin North Am
2003; 29: 61-75.
Shirtliff M E, Mader J T. Acute septic arthritis. Clin Microbiol Rev 2002; 15: 527-544.
Other bone infections
Pott's disease
Pott's disease is tuberculous spondylitis
Well recognised in Egyptian mummies
Described by Percival Pott in 1779
Now rare in western countries
Still prevalent in the developing world
Pathology
Usually occurs secondary to infection elsewhere
Due to a combination of osteomyelitis and arthritis
Often occurs at more than one vertebral level
Usually affects anterior part of vertebral body
More common in thoracic spine
Bone destruction lead to vertebral collapse and kyphosis
Spinal cord can be narrowed resulting in cord compression and neurological deficit
Clinical presentation
Back pain is the commonest symptom
Pain may be present for several months
Pain can be both spinal and radicular
50% patients have neurological signs at presentation
Most patients have some degree of kyphosis
Cold abscess may point in the groin
Investigations
Serum ESR is usually massively raised
Tuberculin skin test is usually positive
Plain x-rays may show
o Lytic destruction of anterior vertebral body
o Anterior vertebral collapse
o Reactive sclerosis
o Enlarged psoas shadow
CT or MRI provides information on disc space and neurological involvement
As allows CT guided biopsy to obtain microbiological and pathological specimens
Picture provided by Christine Breynoert, Hospital Saint-Elizabeth, Zottegen, Belgium
Treatment
Treatment involves both tuberculous chemotherapy and possible surgery
Nine months of combination chemotherapy should be used
This involves 3 or 4 drugs
Isoniazid and rifampicin should be given for full nine months
Pyrazinamide, ethambutol or streptomycin should be give for first 2 months
Surgery is indicated if:
o Neurological deficit
o Spinal deformity with instability
o No response to medical treatment
o Non-diagnostic percutaneous biopsy
Surgical approach depends on extent of disease and level of spinal involvement
Usually involves radical debridement and posterior stabilisation
Bibliography
Almeida A. Tuberculosis of the spine and spinal cord. Eur J Radiol 2005; 55: 193-201.
Busteed S, Beeching N J, Nye F J et al. Tuberculous osteomyelitis: chasing the elusive tubercle.
Hosp Med 2004; 65: 438-439.
Moore S L, Rafii M. Imaging of musculoskeletal and spinal tuberculosis. Radiol Clin North Am
2001; 39: 329-342.
Low back pain and sciatica
Lumbar back pain is one of the commonest causes of chronic disability
Usually due to abnormality of intervertebral discs at L4/5 or L5/S1 level
Pathology
With age nucleus pulposus of disc dries out
Annulus fibrosis also develops fissures
Nuclear material may herniate through annulus
May perforate vertebral end-plate to produce a Schmorl node
Flattening of the disc with marginal osteophyte formation is known as spondylosis
Osteoarthritis may develop in the facet joints
Osteophyte formation may narrow lateral recesses of spinal canal
These can encroach on spinal canal and result in spinal stenosis
Acute herniation of disc contents can occur
Usually occurs to one side of the posterior longitudinal ligament
Posterolateral rupture can compress nerve roots
Central posterior rupture can compress the cauda equina
Acute disc rupture
Can occur at any age
Usually occurs in fit adults between 20-45 years
Clinical features
Presents with acute low back pain on stooping or lifting
Pain often radiates to buttock or leg
May be associated with paraesthesia or numbness in the leg
Cauda equina compression can cause urinary retention
Examination may show a 'sciatic' scoliosis
All back movement is restricted
May be lumbar tenderness and paravertebral spasm
Straight leg raising is often restricted
Neurological examination is essential
L5 root signs include:
o Weakness of hallux extension
o Loss of knee reflex
o Sensory loss over the lateral aspect of the leg and dorsum of the foot
S1 root signs include:
o Weakness of foot plantar flexion
o Loss of ankle reflex
o Sensory loss over the lateral aspect of the foot
Cauda equina compression causes
o Urinary retention
o Loss or perianal sensation
Imaging
Lumbar spine x-ray will exclude other bone lesions
Myelography is a historical investigation
MRI is now the investigation of choice
Management
Bed rest is of unproven benefit
Recovery is not hasten by traction
NSAID provide symptomatic relief
The role of epidural steroid injection is unclear
Chemonucleolysis is less effective than surgical discectomy
Surgery is required if:
o Cauda equina compression - neurosurgical emergency
o Neurological deterioration with conservative management
o Persistent symptoms and neurological signs
Surgical options are:
o Partial laminectomy
o Microdiscectomy
Postoperative rehabilitation and physiotherapy are essential
Facet joint dysfunction
Usually present with recurrent low back pain
Pain often related to physical activity
May be referred to the buttock
Often relieved by lying down
Lumbar spine movement is often good
Neurological signs may be few
Lumbar spine x-rays show narrowing of the disc space
Oblique views may show facet joint malalignment
Treatment includes:
o Physiotherapy
o Analgesia
o Facet joint injections
o Spinal fusion
Spinal stenosis
Narrowing of the spinal canal due to hypertrophy of the posterior disc margin
May be compounded by facet joint osteophyte formation
Spinal stenosis may also be associated with:
o Achondroplasia
o Spondylolisthesis
o Paget's disease
Usually presents with either unilateral or bilateral leg pain
Initiated by standing or walking
Relieved by sitting or leaning forward - 'spinal claudication'
Patient prefers to walk uphill rather than downhill
X-rays often show degenerative spondylolisthesis
Diagnosis can be confirmed by MRI
Often treated conservatively
Surgery involves wide laminectomy and decompression
Spondylolisthesis
Spondylolisthesis means forward shift of the spine
Occurs at L4/L5 or L5/S1 level
Can only occur if facet joint locking mechanism has failed
Classified as:
o Dysplastic - 20%
o Lytic - 50%
o Degenerative - 25%
o Post-traumatic
o Pathological
o Postoperative
In lytic spondylolisthesis the pars interarticularis is in two pieces (spondylolysis)
Vertebral body and superior facet joints subluxate and dislocate forward
Degree of overlap is usually expressed as percentage
Cauda equina or nerve roots may be compressed
Presents with back pain and neurological symptoms
Patients have a characteristic stance
A 'step' in the lumbar spine may be palpable
Diagnosis can be confirmed on a plain x-ray
Most patients improve with conservative management
Surgery may be required if:
o Disabling symptoms
o Progressive displacement more than 50%
o Significant neurological compromise
Anterior or posterior fusion may be required
Bibliography
Deyo R A, Weinstein J N. Low Back Pain. N Engl J Med 2001; 344: 363-370.
Hagen H D, Hilde G, Jamtvedt G, Winnem M. Bed rest for acute low back pain. Cochrane
Database Syst Rev 2000; 2: CD001254.
Koes B W, van Tulder M W, Thomas S. Diagnosis and treatment of low back pain. BMJ 2006;
332: 1430-1434.
Nelemas P J, de Bie R A, de Vet H C, Sturmans F. Injection therapy for subacute and chronic low
back pain. Cochrane Database Syst Rev 2000; 2: CD001824.
van Tulder M W, Scholten R J, Koes D C V, Deyo R A. Non-steroidal anti-inflammatory drugs
for low back pain. Cochrane Database Syst Rev 2000; 2: CD000396.
Spinal cord compression
The clinical features of a spinal cord lesion depend on its rate of development
Trauma produces acute compression with rapidly developing effects
Benign neoplasms can cause substantial compression with little neurological deficit
Anatomy
The spinal cord is shorter than spinal canal
The cord ends at the interspace between the L1 and L2 vertebrae
Below the termination of the cord the nerve roots form the cauda equina
Within cervical spine segmental levels of cord correspond to bony landmarks
Below this level there is increasing disparity between levels
Spinal pathology below L1 presents with only root signs
Aetiology
Trauma - vertebral body fracture or facet joint dislocation
Neoplasia - benign or malignant
Degenerative - prolapsed intervertebral disc, osteophyte formation
Vascular - epidural or subdural haematoma
Inflammatory - rheumatoid arthritis
Infection - tuberculosis or pyogenic infections
Clinical presentation
Clinical features depend on extent and rate of development of cord compression
Motor symptoms include easy fatigue and gait disturbance
Cervical spine disease produces quadriplegia
Thoracic spine disease produces paraplegia
Lumbar spine disease affects L4, L5 and sacral nerve roots
Sensory symptoms include sensory loss and paraesthesia
Light touch, proprioception and joint position sense are reduced
Tendon reflexes are often:
o Increased below level of compression
o Absent at level of compression
o Normal above level of compression
Reflex changes may not coincide with sensory level
Sphincter disturbances are late features of cervical and thoracic cord compression
Cauda equina compression due to central disc prolapse produces:
o Loss of perianal sensation
o 'Root pain' in both legs
o Painless urinary retention
Most patients with surgical treatable causes of spinal compression have spinal pain
Movement induce pain suggests vertebral fracture or collapse
Exquisite tenderness suggests an epidural abscess
Low-grade background pain suggests tumour infiltration or osteomyelitis
Investigation
Plain x-rays may show bone or paravertebral soft tissue disease
Features include vertebral collapse, lytic lesions, loss of pedicle
Integrity of disc may indicate diagnosis
'Good disc = bad news' often indicates malignancy
'Bad disc = good news' may indicate infection
MRI is investigation of choice to define extent of soft tissue disease
Bone scan may indicate pattern and extent of bone pathology
Management
Acute cord compression is a 'surgical' emergency
In those with malignant disease radiotherapy may be treatment of choice
In general, tumour, infection and disc disease produces anterior compression
Surgical decompression should be achieved through an anterior approach
Cervical spine can be approached between larynx medially and carotid sheath laterally
Thoracic spine can be approached through chest by a posterior thoracotomy or costotransversectomy
Bibliography
Abraham J. Management of pain and spinal cord compression in patients with advanced cancer.
Ann Intern Med 1999; 131: 37-46.
Gleave J R W, MacFarlane R. Cauda equina syndrome: what is the relationship between timing of
surgery and outcome? Br J Neurosurg 2002; 16: 325-328.
Healey J H, Brown H K. Complications of bone metastases. Cancer 2000; 88 (Suppl 1): 2940-
2951.
Markman N. Early recognition of spinal cord compression in cancer patients. Cleve Clin Med J
1999; 66: 629-631.
Scoliosis
A scoliosis is an apparent lateral curvature of the spine
It is a triplanar deformity with lateral, anteroposterior and rotational components
Postural scoliosis is secondary to pathology away from the spine (e.g. short leg or pelvic tilt)
Curvature disappears when patient sits down
Structural scoliosis is a non-correctable deformity
Vertebral rotation results in spinal processes swinging to concavity of curve
Secondary changes occur to counterbalance primary deformity
Most cases of structural scoliosis are idiopathic
Can also result from bone, neurological or muscular disease
Clinical features
A scoliosis shows a typical deformity with a skew back and rib hump
The hip normally protrudes on the concave side
The scapula normally protrudes on the convex side
The level and direction of the major curve convexity should be noted
Convexity of curvatures determines the nomenclature of the lesion
e.g. A right thoracic scoliosis has the thoracic spine convex to the right
A balanced deformity keeps occiput in midline
A fixed scoliosis become more obvious on flexion
The younger the child and greater the curvature the worse the prognosis
Radiology
Full length PA and lateral films of the spine are required
Upper and lower ends of spinal curve can be identified
Angle of curvature (Cobb's angle) can be measured
Lateral bending view can assess degree of correctability
Skeletal maturity important as scoliosis can progress during skeletal growth
Idiopathic scoliosis
80% of scoliosies are idiopathic
Patients often have a family history
Many patients have a trivial curvature
About 0.2% of population have greater than 30° of curvature
Age of onset defines three groups as adolescent, juvenile and infantile
Adolescent idiopathic scoliosis
Occurs with an onset older than 10 years
90% patients are female
Progression is not inevitable
With curvature of less than 20° spontaneous resolution can occur
Predictors of progression include young age, marked curvature and skeletal immaturity
Main aim of treatment is to prevent mild deformity becoming severe
If mild scoliosis with progression consider brace
If greater than 30° and progressing operative intervention may be required
Harrington rods used to reduce rotational deformity and lateral curvature
Juvenile idiopathic scoliosis
Occurs with an onset between 4 and 9 years
Relatively uncommon condition
Prognosis is worse than adolescent group
Spinal fusion may be necessary before puberty
Infantile idiopathic scoliosis
Occurs with an onset less than 3 years
Is a rare condition
60% patients are boys
In 90% the deformity resolves spontaneously
In those in whom progression occurs the curvature can be severe
Associated with a high incidence of cardiopulmonary dysfunction
Osteopathic scoliosis
Associated with hemivertebrae, wedged vertebrae and fused vertebrae
Overlying tissue often shows angiomas, naevi and skin dimples
Scoliosis usually mild
Before considering surgery need to exclude and meningomyelocele
Neuropathic / myopathic scoliosis
Associated with polio, cerebral palsy and muscular dystrophy
Scoliosis is typically long and convex towards side of muscle weakness
X-rays with traction with assess the degree of correctability
Bibliography
Bridewell K H. Surgical treatment of idiopathic adolescent scoliosis. Spine 1999; 24: 2607-2616.
Dobbs M B, Weinstein S L. Infantile and juvenile scoliosis. Orthop Clin North Am 1999; 30: 331-
341.
Sarwark J F, Kramer A. Pediatric spinal deformity. Curr Opin Pediatr 1998; 10: 82-86.
Weinstein S L, Dolan L A, Cheng J C et al. Adolescent idiopathic scoliosis. Lancet 2008; 371:
1727-1537.
Thoracic outlet compression syndrome
Describes a collection of upper limb neurological and vascular symptoms
Arise from proximal compression of neurovascular structures
Usually affects middle aged women
Male : female ratio is 1:3
10% have bilateral symptoms
Pathophysiology
Compression can result from a bone, muscle or fibromuscular band
Compressing lesion is usually congenital
30% of cases follow trauma (e.g. whiplash injury)
Clinical features
Neurological features are more common than vascular
Subclavian artery aneurysm and axillary vein thrombosis are uncommon
Symptoms often worsened by carrying weights or lifting arms above head
Differential diagnosis includes:
o Cervical spondylosis
o Distal nerve compression
o Pancoast's tumour
o Connective tissue disorders
o Vascular and venous embolic disease
Diagnosis depends mainly on the history
Signs are few but diagnosis may be confirmed with the
o Roos test - Reproduction of symptoms with arms flexed and abducted
o Subclavian compression tests (e.g. Adson's manoeuvre)
o Loss of radial pulse with head turned to opposite side and neck extended
Investigations
The results of investigations are often normal
A CXR may show a cervical rib
Nerve conduction studies may be needed to exclude a distal nerve compression
Arch aortogram may show a subclavian artery aneurysm
Duplex scanning may show arterial or venous compression and the effect of position
Picture provided by Andrew McIrvine, Darent Valley Hospital, Dartford, United Kingdom
Treatment
Symptoms may improve with physiotherapy
If disabling symptoms need to consider surgical decompression
Involves resection of most of first rib
Can be achieved through either a supraclavicular or transaxillary approach
10% will develop a pneumothorax
Prognosis
80% report a symptomatic improvement
More than 50% of patients are usually symptom free
Failure to improve is often due to:
o A double crush compression syndrome
o Incomplete division of compressing structure
Bibliography
Edwards D P, Mulkern E, Raja A N, Barker P. Trans-axillary first rib excision for thoracic outlet
syndrome. J R Coll Surg Ed 1999; 44: 362-365.
Thompson R W, Petrinec D. Surgical treatment of thoracic outlet compression syndromes:
diagnostic considerations and transaxillary first rib resection. Ann Vasc Surg 1997; 11: 315-323.
Urschel H C, Razzuk M A. Neurovascular compression in the thoracic outlet: changing
management over 50 years. Ann Surg 1998; 228: 609-617.
Primary bone tumours
Primary bone tumours are rare
Secondaries tumours are more common especially in the elderly
Classification
Cell type Benign Malignant
Bone Osteoid osteoma Osteosarcoma
Cartilage Chondroma Chondrosarcoma
Osteochondroma
Fibrous tissue Fibroma Fibrosarcoma
Bone marrowEosinophilic
granulomaEwing's sarcoma
Myeloma
Vascular Haemangioma Angiosarcoma
Uncertain Giant-cell tumour Malignant giant cell tumour
Clinical features
Most present with pain, swelling and localised tenderness
Rapid growth and erythema are suggestive of malignancy
May cause pathological fractures
Diagnosis confirmed by:
o Plain x-ray
o CT scan
o Bone scan
o Carefully planned biopsy
Osteoid osteoma
Benign bone tumour
Usually less than 1 cm in diameter and surround by dense osteoid
Occurs in young adults
Tibia and femur are the commonest site
Pain (relieved by aspirin) is presenting complaint
Xray has characteristic appearance of a radiolucency surrounded by dense bone
Local excision is curative
Osteochondroma
Commonest bone tumour
Lesions can be single or multiple
Appears in adolescence as cartilaginous overgrowth at epiphyseal plate
Grows with underlying bone
Metaphyses of long bones are the commonest sites
Presents as painless lump or occasionally joint pain
Excision should be considered if causing significant symptoms
Chondroma
Benign tumour of cartilage
Lesions may be single or multiple (Ollier's disease)
Appears in tubular bones of hands and feet
Xray shows well defined osteopenic area in the medulla
Lesion should excised and bone grafted
Giant-cell tumour (Osteoclastoma)
Equal proportions are benign, locally invasive and metastatic
Found in sub-articular cancellous region of long bones
Only occurs after closure of epiphyses
Patients are usually between 20 and 40 years
Xray shows an asymmetric rarefied area at the end of a long bone
Cortex is thinned or even perforated
Treatment by local excision and grafting often leads to recurrence
Wide excision and joint replacement is the treatment of choice
Amputation if malignant or recurrent tumour
Osteosarcoma
Occurs in the metaphyses of long bones
Commonest sites are around the knee or proximal humerus
Destroys bone and spreads into the surrounding tissue
Rapidly metastasizes to the lung
Usually occurs between 10 and 20 years
In later life is seen associated with Paget's disease
X-ray shows combination of bone destruction and formation
Periosteum may be lifted (Codman's triangle)
Soft tissue calcification produces a 'sunburst' appearance
Treatment involves amputation and chemotherapy
Amputations are often limited with prosthetic replacement
50% five years survival
Worst prognosis seen with proximal and axial skeletal lesions
Picture provided by Sathar Thajam, Monkland's Hospital, Airdrie, Scotland
Chondrosarcoma
Occurs in two forms
'Central' tumour in pelvis or proximal long bones
'Peripheral' tumour in the cartilaginous cap of an osteochondroma
Tend to metastasise late
Wide local excision is often possible
Bibliography
Ham S J, Schraffordt-Koops H, van der Graaf W T, van Horn J R, Postma L, Hoekstra H J.
Historical, current and future aspects of osteosarcoma treatment. Eur J Surg Oncol 1998; 24: 584-
600.
Witt J. Management of osteoid osteoma. Hosp Med 2002; 63: 207-209.
Bone metastases
30% of patients with malignant disease will develop bone metastases
10% of these patients will develop a pathological fracture
Tumours spread to bone by:
o Direct invasion
o Haematogenous spread
o Lymphatic spread
o Spread via paravertebral venous plexus
Commonest sites lumbar vertebrae, pelvis and ribs
Primary tumours which spread to bone
Breast (35%)
Prostate (30%)
Bronchus (10%)
Kidney (5%)
Thyroid (2%)
Others (18%)
Clinical features
Pain or localised bone lump
Pathological fracture
Hypercalcaemia
Cord compression
Radiology
Plain x-rays can be normal
If abnormal will show either an osteolytic or sclerotic lesion
Bone scan has higher sensitivity than x-rays
May identify other asymptomatic lesions
Differential diagnosis
Calcified enchondroma
Hyperparathyroidism
Chronic sclerosing osteomyelitis
Bone infarct
Myeloma deposit
Treatment
The aims of treatment are to relieve pain and preserve mobility
If pathological fracture consider internal fixation for early mobilisation and pain relief
Consider radiotherapy for back pain
Spinal decompression may be needed for cord compression
Prophylactic internal fixation may be required if:
o Greater than 50% erosion of a long bone cortex
o A metastasis of more than 2.5 cm in diameter
o Metastasis in high risk area (e.g. subtrochanteric femur)
o Metastasis with persistent pain
Bibliography
British Association of Surgical Oncology Guideline. The management of metastatic bone disease in
the United Kingdom. The Breast Speciality Group of the British Association of Surgical Oncology.
Eur J Surg Oncol 1999; 25: 3-23.
Downey S E, Bundred N J. Bone metastases. In: Johnson C D, Taylor I eds. Recent advances in
surgery 19. Churchill Livingstone, Edinburgh 1996; 109-128.
Major P P, Cook R. Efficacy of bisphosphonates in the management of skeletal complications of
bone metastases and selection of clinical end-points. Am J Clin Oncol 2002; 25 (Suppl1); S10-S18.
Radford M, Gibbons C L. Management of skeletal metastases. Hosp Med 2002; 63: 722-725
Rosenthal D I. Radiologic diagnosis of bone metastases. Cancer 1997; 80 (Suppl 8): 1595-1607.
Ryan P J. Fogelman I. The bone scan: where are we now? Semin Nucl Med 1995; 25: 76-91.
Multiple myeloma
Multiple myeloma is a malignant disease of plasma cells in bone marrow
Accounts for 1% of all cancers
2,500 new cases each year in United Kingdom
Most patients are over 60 years of age
Characterised by production of monoclonal immunoglobulins
These can be detected in serum, urine or both
Pathogenesis
Monoclonal overgrowth of one clone of plasma cells occurs
Produces monoclonal immunoglobulin or paraprotein
In 80% patients an IgG or IgA is detectable in serum
In 20% no paraprotein is detectable in the serum
Free light chains may cross glomerulus and appear in urine
These are known as Bence-Jones proteins
Clinical features
Bone pain - especially back pain
Pathological fracture
Cord compression may occur
Hypercalcaemia
Renal failure
Anaemia
Immunosuppression
Amyloidosis
Investigations
Diagnosis confirmed by:
o Paraprotein in serum or urine on electrophoresis
o Lytic lesions on radiography
o Bone marrow aspirate with more than 10% plasma cells
Management
70% patients respond to therapy
Complete remission is rare
Median survival is 3 years
Treatment options
o Melphalan chemotherapy
o Interferon-alpha
o Bone marrow transplantation
Treatment of complications
o Dialysis for renal failure
o Bisphosphonates for hypercalcaemia
o Radiotherapy for localised bone pain
Bibliography
Bataille R, Harousseau J L. Multiple myeloma. N Engl J Med 1997; 336: 1657-1663.
Berenson J, Lichtenstein A, Porter L et al. Efficacy of pamidronate in reducing skeletal events in
patients with advanced multiple myeloma. N Engl J Med 1996; 334: 488-493.